Propofol abuse in academic anesthesiology likely has increased over the last 10 yr. Much of the mortality is in residents. Most programs have no pharmacy accounting or control of propofol stocks. This may be of concern, given that all programs reporting deaths from propofol abuse were centers in which there was no pharmacy accounting for the drug.
Canine COX-2 was selectively inhibited by etodolac, nimesulide, and NS398; tolfenamic acid and carprofen also appeared to be preferential COX-2 inhibitors in dogs. The roles of COX-1 as a constitutive housekeeping enzyme and COX-2 as a proinflammatory inducible enzyme (as determined in humans) appear to apply to dogs; therefore, COX-2-selective inhibitors should prove useful in reducing the adverse effects associated with nonselective NSAIDs.
SummaryThis study aims to assess the prevalence and outcomes of inhalational anaesthetic abuse among anaesthesia training programmes. Online surveys were completed by chairpersons of academic anaesthesia training programmes in the United States. The response rate was 84% (106 ⁄ 126 programmes). Twenty-two percent of the departments had had at least one incident of inhalational anaesthetic abuse. Forty-eight percent (15 ⁄ 31) of the persons abusing inhalational anaesthetics were sent for rehabilitation. Only 22% (7 ⁄ 31) of those found to be abusing inhalational anaesthetics were ultimately able to return successfully to anaesthesia practice with sustained recovery. The mortality rate among individuals found abusing inhalational anaesthetics was 26% (8 ⁄ 31). The majority of the anaesthesia departments (97 ⁄ 104, 93%) did not have any pharmacy accounting of inhalational anaesthetics. This is the first published survey of inhalational anaesthesia abuse. Inhalational anaesthetic abuse should be considered in at-risk individuals or those with a history of substance abuse. The concern about substance abuse is not unique to American anaesthetists. Countries around the world deal with similar substance abuse issues.
IntroductionPharmacological agents that block beta-adrenergic receptors have been associated with improved outcome in burn injury. It has been hypothesized that injuries leading to a hypermetabolic state, such as septic shock, may also benefit from beta-blockade; however, outcome data in experimental models have been contradictory. Thus, we investigated the effect of beta-blockade with propranolol on survival, hemodynamics, lung heat shock protein (HSP) expression, metabolism and inflammatory markers in a rat cecal ligation and puncture (CLP) model of sepsis.MethodsSprague-Dawley rats receiving either repeated doses (30 minutes pre-CLP and every 8 hours for 24 hours postoperatively) of propranolol or control (normal saline), underwent CLP and were monitored for survival. Additionally, lung and blood samples were collected at 6 and 24 hours for analysis. Animals also underwent monitoring to evaluate global hemodynamics.ResultsSeven days following CLP, propranolol improved survival versus control (P < 0.01). Heart rates in the propranolol-treated rats were approximately 23% lower than control rats (P < 0.05) over the first 24 hours, but the mean arterial blood pressure was not different between groups. Metabolic analysis of lung tissue demonstrated an increase in lung ATP/ADP ratio and NAD+ content and a decreased ratio of polyunsaturated fatty acids to monounsaturated fatty acids (PUFA/MUFA). Cytokine analysis of the inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) demonstrated decreased expression of TNF-alpha in both lung and plasma at 24 hours post CLP induced sepsis. Finally, propranolol led to a significant increase in lung hemeoxygenase-1 expression, a key cellular protective heat shock protein (HSP) in the lung. Other lung HSP expression was unchanged.ConclusionsThese results suggest that propranolol treatment may decrease mortality during sepsis potentially via a combination of improving metabolism, suppressing aspects of the inflammatory response and enhancing tissue protection.
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